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Beta-Blockers

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Beta-blockers xxxx Collin College
HPRS 1310-WW1
April 15, 2012

The first beta-blocker drug approved by the FDA in 1967 was developed by Sir James Black, an accomplishment for which he was awarded the Nobel Prize in Medicine in 1988 (Stapleton, 1997). Sir Black took a different approach to the treatment of angina pectoris—instead of using drugs to increase the amount of oxygen delivered to the heart, Black sought to find a drug that could reduce the amount of oxygen required by the heart.
The drugs in this classification are subdivided into two categories: non-selective and selective (cardioselective). Major drugs in the non-selective beta-blocker category include carteolol, nadolol, penbutolol, pindolol, propranolol, sotalol, and timolol. Major drugs in the cardioselective category include acebutolol, atenolol, betaxolol, esmolol, metroprolol, and nebivolol. Some others, including carvedilol and labetalol also have alpha-adrenergic blocking effects, but are outside the scope of this paper. (Vallerand, 2013; Turley, 2010) Beta-blockers are prescribed for the treatment of hypertension, angina pectoris, cardiac arrhythmias, hypertrophic subaortic stenosis, prevention of myocardial infarction, congestive heart failure, migraine headaches, and glaucoma. (Vallerand, 2013; Hodgson & Kizior, 2013) Beta-blockers work to compete with sympathetic neurotransmitters1 for beta1 and beta2 adrenergic receptor sites. Beta1 receptors are found in cardiac muscle, and beta2 receptors in vascular, bronchiolar, and uterine smooth muscle. Stimulation of beta1 receptors causes an increase in heart rate and contractility. Stimulation of beta2 receptors triggers vasoconstriction2 (which causes an increase in blood pressure), and bronchiodilation3. Blocking these receptor sites keeps epinephrine from stimulating them, and thus causes the opposite effect of their stimulation: decrease in heart rate and contractility, and vasodilation and bronchioconstriction. Hypertension is characterized by blood pressure over 120/80mm Hg (Turley, 2010). Both non-selective and cardioselective beta-blockers decrease heart rate and contractility, and dilate the blood vessels, thereby decreasing blood pressure. Cardioselective beta-blockers are prescribed to asthmatic patients to avoid the effects of bronchioconstriction due to blockage of beta2 receptors in the lungs. Beta-blockers’ effect of slowing heart rate and contractility is also used to treat both tachycardia4 and atrial flutter and fibrillation5. When heart rate is decreased, so is the amount of oxygen required by the heart. Decreasing the amount of oxygen required by the heart decreases the pain of angina pectoris6. Therefore, the beta-blockers atenolol, metoprolol, nadolol, and propranolol are prescribed to reduce the pain associated with angina pectoris. Reduction of heart rate and vasodilation help to relieve the strain on the heart, and therefore beta-blockers are prescribed to treat hypertrophic subaortic stenosis7, congestive heart failure8 and to prevent myocardial infarction9. Though their mechanism of action is poorly understood in the prevention of migraine headaches, five beta-blockers are commonly prescribed: atenolol, metoprolol, nadolol, propranolol, and timolol. When applied to the eyes, beta blockers decrease the intraocular pressure associated with glaucoma10 by decreasing the production of aqueous humor11. Patients with the above mentioned heart problems and/or hypertension should experience a decrease in blood pressure, along with a decrease in heart rate and contractility when treated with beta-blockers. These effects lead to an overall decrease in morbidity and mortality in these patients (Butler et al, 2006). Studies have shown that treatment with beta-blockers, along with behavioral management is effective in the prevention of recurring migraine headaches (Holroyd et al, 2010). When treated with beta-blockers, patients with glaucoma should experience a decrease in intraocular pressure, which will relieve pressure on the optic nerve, thereby preventing the loss of vision. Treatment with beta-blockers cannot reverse any loss of vision already experienced, but can help to prevent further loss of vision.
Beta-blockers are most commonly administered orally (available in tablet, capsule, and solution forms), and can also be administered intravenously. When treating glaucoma, beta-blockers are applied topically to the eyes in the form of drops. Side effects may include dizziness, light-headedness, blurred vision, and drowsiness. A chilled feeling may occur, especially at the extremities, due to reduced circulation. Known adverse effects include congestive heart failure, bronchospasm, and bradyarrythmias12. Patients should not abruptly discontinue use of beta-blockers, as it could cause life-threatening hypertension or arrhythmias. In addition to following medication instructions, patients are given instructions for weight loss, diet adjustments including reduction of sodium, exercise, stopping smoking, and stress management. Patients should regularly monitor their blood pressure, and report changes to their doctor. Patients should consult their doctor before taking any over the counter medications, as well as disclose all medications to their doctor before beginning beta-blocker therapy. Patients are advised to carry identification that indicates their current medication regimen. Beta-blockers are obviously a well-established method of therapy for so many heart and blood pressure illnesses. They are one of the most important breakthroughs in pharmacology, and have no doubt lengthened and/or improved the quality of countless lives.

Medical Terminology 1. sympathetic neurotransmitters—The sympathetic nervous system is a branch of the body’s autonomic nervous system, which “automatically” controls body functions. The sympathetic division is responsible for “fight-or-flight” type reactions. Sympathetic neurotransmitters stimulate specific cell receptors in order to bring about these “fight-or-flight” reactions. 2. vasoconstriction—constriction of blood vessels 3. bronchiodilation—dilation of bronchioles of the lungs 4. tachycardia—a faster than normal, but consistent, heart beat 5. flutter and fibrillation—irregular patterns of rapid heart beat 6. angina pectoris—a condition that causes chest pain that can be caused by a buildup of plaques in the coronary arteries, vasoconstriction of coronary arteries, or spasm of the coronary arteries, which causes a lack of oxygen to the heart muscle 7. hypertrophic subaortic stenosis—a heart condition often caused by a thickening of the heart muscle which causes a decrease in cardiac output 8. congestive heart failure--weakened heart muscle due to diseased or defective heart tissue 9. myocardial infarction—heart attack 10. glaucoma—a condition where too much aqueous humor11 is produced in the eye, which puts pressure on the optic nerve, which could cause loss of vision 11. aqueous humor—liquid in the chamber of the eye between the cornea and lens 12. bradyarrhythmia—irregularly occurring slower than normal heart rate

References
Butler, J., Young, J.B., Abraham, W.T., Bourge, R.C., Adams, Jr., K.F., & Clare, R., O’Connor, C. (2006). Beta-Blocker Use and Outcomes Among Hospitalized Heart Failure. Journal of the American College of Cardiology 47(12): 2462-9.
Hodgson, B.B., & Kizior, R.J. (Eds.) (2013). Saunders nursing drug handbook. St. Louis, MO: Elsevier.

Holroyd K.A., Cottrell C.K., O'Donnell F.J., Cordingley G.E., Drew J.B., Carlson B.W., & Himawan L. (2010). Effect of preventive (beta blocker) treatment, behavioural migraine management, or their combination on outcomes of optimised acute treatment in frequent migraine: randomised controlled trial. British Medical Journal 341(c4871). doi:10.1136.
Stapleton, M.P. (1997) Sir James Black and propranolol: The role of the basic sciences in the history of cardiovascular pharmacology. Texas Heart Institute Journal 24(4): 336-42.

Turley, S.M., (2010). Understanding pharmacology for health professionals – 4th ed. Upper Saddle River, NJ: Pearson Education, Inc.
Vallerand, A.H., Sanoski, C.A., Deglin,J.H. (Eds.) (2013). Davis's drug guide for nurses - 13th Ed. Philadelphia, PA: F. A. Davis Company.

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